Correlation of Probe-Based Confocal Laser Endomicroscopy (pCLE) and Mucosal Integrity Testing (MIT) with Epithelial Barrier Function and Presence of Gastroesophageal Reflux Disease (GERD).

Introduction: Epithelial barrier function (EBF) disruption is a key mechanism underlying gastroesophageal reflux disease (GERD). Our aim was to assess whether two novel technologies, probe-based confocal laser endomicroscopy (pCLE) and mucosal integrity testing (MIT), could assess EBF.

Methods: We prospectively enrolled patients undergoing upper endoscopy for refractory GERD or non-GERD conditions.

Proton pump inhibitors: misconceptions and proper prescribing practice.

Purpose Of Review: The current review summarizes and attempts to place in proper perspective the past year's literature regarding purported adverse effects of proton pump inhibitors (PPIs).

Recent Findings: Although generally considered safe, physicians are inundated with retrospective database-driven epidemiologic studies, and meta-analyses on the same studies, claiming a panoply of serious adverse effects associated with long-term use of PPIs. The quality of the evidence underlying most of these associations is very low and cannot ascribe cause and effect.

Gastric Peptides-Gastrin and Somatostatin.

Gastric acid secretion (i) facilitates digestion of protein as well as absorption of micronutrients and certain medications, (ii) kills ingested microorganisms, including Helicobacter pylori, and (iii) prevents bacterial overgrowth and enteric infection. The principal regulators of acid secretion are the gastric peptides gastrin and somatostatin. Gastrin, the major hormonal stimulant for acid secretion, is synthesized in pyloric mucosal G cells as a 101-amino acid precursor (preprogastrin) that is processed to yield biologically active amidated gastrin-17 and gastrin-34.

Proton pump inhibitors: placing putative adverse effects in proper perspective.

Purpose Of Review: This review summarizes the past year's literature, both clinical and basic science, regarding potential adverse effects of proton pump inhibitors (PPIs).

Recent Findings: PPIs are amongst the most widely prescribed and over-prescribed medications worldwide. Although generally considered well tolerated, epidemiologic studies that mine large databases have reported a panoply of putative adverse effects associated with PPIs.

Adverse effects of proton pump inhibitors: fact or fake news?

Purpose Of Review: The present review summarizes the past year's literature, both clinical and basic science, regarding potential adverse effects of proton pump inhibitors.

Recent Findings: Proton pump inhibitors are amongst the most widely prescribed and overprescribed medications worldwide. Although generally considered well tolerated, epidemiologic studies mining large databases have reported a panoply of purported serious adverse effects associated with proton pump inhibitors, including chronic kidney disease, cognitive decline, myocardial infarction, stroke, bone fracture and even death.

Proton Pump Inhibitor Initiation and Withdrawal affects Gut Microbiota and Readmission Risk in Cirrhosis.

Objectives: Cirrhosis is associated with gut microbial dysbiosis, high readmissions and proton pump inhibitor (PPI) overuse, which could be inter-linked. Our aim was to determine the effect of PPI use, initiation and withdrawl on gut microbiota and readmissions in cirrhosis.

Methods: Four cohorts were enrolled.

Gastric acid suppression promotes alcoholic liver disease by inducing overgrowth of intestinal Enterococcus.

Chronic liver disease is rising in western countries and liver cirrhosis is the 12th leading cause of death worldwide. Simultaneously, use of gastric acid suppressive medications is increasing. Here, we show that proton pump inhibitors promote progression of alcoholic liver disease, non-alcoholic fatty liver disease, and non-alcoholic steatohepatitis in mice by increasing numbers of intestinal Enterococcus spp.

Physiologic, pathophysiologic, and pharmacologic regulation of gastric acid secretion.

Purpose Of Review: The present review summarizes the past year's literature, both clinical and basic science, regarding physiologic and pharmacologic regulation of gastric acid secretion in health and disease.

Recent Findings: Gastric acid kills microorganisms, assists digestion, and facilitates absorption of iron, calcium, and vitamin B12. The main stimulants of acid secretion are the hormone gastrin, released from antral G cells; paracrine agent histamine, released from oxyntic enterochromaffin-like cells; and neuropeptide acetylcholine, released from antral and oxyntic intramural neurons.

Helicobacter pylori-Induced Changes in Gastric Acid Secretion and Upper Gastrointestinal Disease.

Appropriate management of Helicobacter pylori infection of the human stomach is evolving and remains a significant clinical challenge. Acute infection results in hypochlorhydria, whereas chronic infection results in either hypo- or hyperchlorhydria, depending upon the anatomic site of infection. Acute hypochlorhydria facilitates survival of the bacterium and its infection of the stomach.

Gastric acid secretion.

Purpose Of Review: The present review summarizes the past year's literature, both clinical and basic science, regarding neuroendocrine and intracellular regulation of gastric acid secretion and proper use of antisecretory medications.

Recent Findings: Gastric acid kills microorganisms, modulates the gut microbiome, assists in digestion of protein, and facilitates absorption of iron, calcium, and vitamin B12. The main stimulants of acid secretion are gastrin, released from antral G cells; histamine, released from oxyntic enterochromaffin-like cells; and acetylcholine, released from antral and oxyntic intramural neurons.

Functional anatomy and physiology of gastric secretion.

Purpose Of Review: This review summarizes the past year's literature regarding the neuroendocrine and intracellular regulation of gastric acid secretion, discussing both basic and clinical aspects.

Recent Findings: Gastric acid facilitates the digestion of protein as well as the absorption of iron, calcium, vitamin B12, and certain medications. High acidity kills ingested microorganisms and limits bacterial overgrowth, enteric infection, and possibly spontaneous bacterial peritonitis.

Systems biology analysis of omeprazole therapy in cirrhosis demonstrates significant shifts in gut microbiota composition and function.

Proton pump inhibitors (PPI) have been associated with infectious complications in cirrhosis, but their impact on distal gut microbiota composition and function is unclear. We aimed to evaluate changes in stool microbiota composition and function in patients with cirrhosis and healthy controls after omeprazole therapy. Both 15 compensated cirrhotic patients and 15 age-matched controls underwent serum gastrin measurement, stool microbiota profiling with multitagged pyrosequencing, and urinary metabolic profiling with NMR spectroscopy to assess microbial cometabolites before/after a 14-day course of 40 mg/day omeprazole under constant diet conditions.

Gastric secretion.

Purpose Of Review: This review summarizes the past year's literature regarding the neural, paracrine, hormonal, and intracellular regulation of gastric acid secretion.

Recent Findings: Gastric acid facilitates the digestion of protein as well as the absorption of iron, calcium, vitamin B12, and certain medications. High gastric acidity, in combination with pepsin and lipase, kills ingested microorganisms and may play a role in preventing bacterial overgrowth, enteric infection, and possibly spontaneous bacterial peritonitis, community-acquired pneumonia, and infection with Mycobacterium tuberculosis.